Zhang Xin-yu, Zhou Chu-song, Jin An-min, Tian Jing, Zhang Hui, Yao Wei-tao, Zheng Gang
Department of Orthopedics, Zhujiang Hospital, First Military Medical University, Guangzhou 510282, China.
Di Yi Jun Yi Da Xue Xue Bao. 2003 Jul;23(7):687-9.
To study the effects of aminoguanidine (AG), the inhibitor of inducible nitric oxide synthase (NOS), on the recovery of rat hindlimb motor function after spinal cord injury and explore the possible mechanism.
Thirty rat models of spinal cord compression injury were established according to Nystrom's method. AG therapy was administered for 4 times at 1 h before and 8, 24, 36 h after the injury, and 24 h after the completion of the therapy, spectrophotography was performed to measure the content of NO and activity of NOS in the injured spinal cord, followed by flow cytometry for determining the apoptotic rate 48 h later. The evaluation of the hindlimb motor function recovery was conducted by electrophysiological method and by measuring the behavior scores.
AG significantly decreased the NO content (from 2.2714+/-0.4239 micromol/g.pro to 0.8466+/-0.0477 micromol/g.pro, P <0.05) and NOS activity (from 0.3408+/-0.0228 U/mg pro to 0.2702+/-0.0148 U/mg pro, P <0.05) in the injured spinal cord. The apoptotic rats were also reduced (from 7.88% +/-0.79% to 3.10% +/-0.66%, P <0.05). Four weeks after the therapy, the behavior score of the rats improved from 7.1+/-4.5 to 17.3+/-4.7 (P <0.01), and the latency and amplitude of the motor evoked potentials improved from 0 ms to 8.89+/-0.91 ms and from 0 mv to 1.99+/-0.48 mv respectively, showing significant therapeutic effect of AG (P <0.05).
AG can improve motor functions of injured spinal cord in rats, possibly resulting from decreased apoptotic cells of the neurons in the spinal cord in the early stages of the injury.
研究诱导型一氧化氮合酶（NOS）抑制剂氨基胍（AG）对脊髓损伤大鼠后肢运动功能恢复的影响，并探讨其可能机制。
按照Nystrom法建立30只大鼠脊髓压迫损伤模型。在损伤前1小时及损伤后8、24、36小时给予AG治疗4次，治疗结束后24小时，采用分光光度法测定损伤脊髓中NO含量和NOS活性，随后在48小时后通过流式细胞术测定凋亡率。采用电生理方法并测量行为评分对后肢运动功能恢复进行评估。
AG显著降低了损伤脊髓中的NO含量（从2.2714±0.4239微摩尔/克蛋白降至0.8466±0.0477微摩尔/克蛋白，P<0.05）和NOS活性（从0.3408±0.0228单位/毫克蛋白降至0.2702±0.0148单位/毫克蛋白，P<0.05）。凋亡大鼠数量也减少（从7.88%±0.79%降至3.10%±0.66%，P<0.05）。治疗4周后，大鼠行为评分从7.1±4.5提高到17.3±4.7（P<0.01），运动诱发电位的潜伏期和波幅分别从0毫秒提高到8.89±0.91毫秒和从0毫伏提高到1.99±0.48毫伏，显示AG具有显著治疗效果（P<0.05）。
AG可改善大鼠脊髓损伤后的运动功能，可能是由于损伤早期脊髓神经元凋亡细胞减少所致。
